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miR-Let7A Modulates Autophagy Induction in LPS-Activated Microglia
Microglia regulate the secretion of various immunomediators in central nervous system diseases. Microglial autophagy is the crucial process for cell's survival and cytokine productions. Recent studies have reported that several microRNAs are involved in the autophagy system. miR-Let7A is such a...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Korean Society for Brain and Neural Science
2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4479807/ https://www.ncbi.nlm.nih.gov/pubmed/26113790 http://dx.doi.org/10.5607/en.2015.24.2.117 |
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author | Song, Juhyun Oh, Yumi Lee, Jong Eun |
author_facet | Song, Juhyun Oh, Yumi Lee, Jong Eun |
author_sort | Song, Juhyun |
collection | PubMed |
description | Microglia regulate the secretion of various immunomediators in central nervous system diseases. Microglial autophagy is the crucial process for cell's survival and cytokine productions. Recent studies have reported that several microRNAs are involved in the autophagy system. miR-Let7A is such a microRNA that plays a role in various inflammation responses, and is magnified as a key modulator particularly in the autophagy system. In present study, we investigated whether miR-Let7A is involved in autophagy in activating microglia. Overexpression of miR-Let7A in LPS-stimulated BV2 microglial cells promoted the induction of the autophagy related factors such as LC3II, Beclin1, and ATG3. Our results suggest a potential role of miR-Let7A in the autophagy process of microglia during CNS inflammation. |
format | Online Article Text |
id | pubmed-4479807 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | The Korean Society for Brain and Neural Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-44798072015-06-25 miR-Let7A Modulates Autophagy Induction in LPS-Activated Microglia Song, Juhyun Oh, Yumi Lee, Jong Eun Exp Neurobiol Original Article Microglia regulate the secretion of various immunomediators in central nervous system diseases. Microglial autophagy is the crucial process for cell's survival and cytokine productions. Recent studies have reported that several microRNAs are involved in the autophagy system. miR-Let7A is such a microRNA that plays a role in various inflammation responses, and is magnified as a key modulator particularly in the autophagy system. In present study, we investigated whether miR-Let7A is involved in autophagy in activating microglia. Overexpression of miR-Let7A in LPS-stimulated BV2 microglial cells promoted the induction of the autophagy related factors such as LC3II, Beclin1, and ATG3. Our results suggest a potential role of miR-Let7A in the autophagy process of microglia during CNS inflammation. The Korean Society for Brain and Neural Science 2015-06 2015-06-17 /pmc/articles/PMC4479807/ /pubmed/26113790 http://dx.doi.org/10.5607/en.2015.24.2.117 Text en Copyright © Experimental Neurobiology 2015. http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Song, Juhyun Oh, Yumi Lee, Jong Eun miR-Let7A Modulates Autophagy Induction in LPS-Activated Microglia |
title | miR-Let7A Modulates Autophagy Induction in LPS-Activated Microglia |
title_full | miR-Let7A Modulates Autophagy Induction in LPS-Activated Microglia |
title_fullStr | miR-Let7A Modulates Autophagy Induction in LPS-Activated Microglia |
title_full_unstemmed | miR-Let7A Modulates Autophagy Induction in LPS-Activated Microglia |
title_short | miR-Let7A Modulates Autophagy Induction in LPS-Activated Microglia |
title_sort | mir-let7a modulates autophagy induction in lps-activated microglia |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4479807/ https://www.ncbi.nlm.nih.gov/pubmed/26113790 http://dx.doi.org/10.5607/en.2015.24.2.117 |
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